GI Motility Flashcards
(78 cards)
1
Q
Which parts of digestive tract are part of digestive period? Intergestive period?
A
Digestive period: Stomach (relaxation, accommadation, gastric emptying) and small intestine (segmentation: slow movement).
Interdigestive period: Stomach: migrating myoelectric complexes (MMC) and Small intestine MMC (perestalsis)
2
Q
Digestive or interdigestive period produces the strongest contractions.
A
Interdigestive period
3
Q
Describe times during which food stays in each part of the digestive tract.
A
Mouth: Seconds
Swallowing: 10-15 seconds
Stomach (resident time): 2-4 hours. Digestive period
Small intestine (transient time): 2-4 hours. Digestive period. In other words, digestive period can take up to 8 hours!
Emptying stomach/small intestine: 10-18 hours (interdigestive period)…..also note there is an additional motility period (migrating myoelectric complex) of 1.5 hours. The hours determined by the amount of meals you eat.
Large intestine: 42-52 hours, minimum of 8-12 hours. Note that large intestine a fecal matter storage site. Food s HIGH IN FIBER pass through QUICKER. American diets (not high in fiber) pass through slower.
Defacation: seconds to minutes
4
Q
When preparing for surgery, which parts of the body must be empty to prevent aspiration during anesthsia?
A
Need enough time to empty the stomach and the small intestine.
5
Q
To prevent aspiration, how long should a patient fast before a surgery requiring general anesthesia?
A
Overnight (2-4 hours for stomach + 2-4 hours for small intestin, so 8 hours is the safest bet). Too short is too risky and too long is unnecessary.
6
Q
Describe the muscles of the GI tract.
A
From the middle of the esophagus all the way tot he rectum: smooth muscle
From mouth to mid esophagus: skeletal muscle.
7
Q
What are the important properties of GI smooth muscle?
A
- High elasticity: allows for significant stretch with relatively low pressure increase. You can eat a crap ton of food, and it will stretch out your stomach. but, the pressure increase is minimal.
- Electric control activity (ECA): regulates smooth muscle contraction and relaxation.
8
Q
Describe the 3 phases of swallowing.
A
- Oral phase (involuntary or voluntary control)
- Pharyngeal phase (involuntary)
- Esophageal phase (involuntary)
9
Q
What organs are involved in swallowing?
A
Mouth, pharynx, esophagous, stomach, RESPIRATORY SYSTEM. All of this is coordinated by CNS.
10
Q
Can you breath and swallow?
A
No. Your breathing is actually the first thing that stops when you are about to swallow, otherwise food gets into the lungs (trachea).
11
Q
What are the steps in pharyngeal and esophageal phases
A
- Stop breathing.
- Upper esophageal sphincter relaxes (opens), lowering its pressure. Same thing happens soon after in lower esophageal sphincter. and
- Fundus of stomach relaxes.
- Back of tongue move the bolus and puts it in the PHARYNX, triggering rapid sequential contraction.
- Since upper esophageal sphincter is open (as well as the lower one), the bolus enters the esophagus and triggers a contractile wave all the way through lower esophageal sphincter into fundus of stomach.
- Respiration resumes, lower esophageal sphincter closes again.
12
Q
Receptive relaxation
A
Relaxation of fundus of stomach prior to the arrival of food.
13
Q
Primary esophageal peristalsis
A
Sequential contraction of esophageal muscle from top to bottom.
14
Q
Explain process of esophageal peristalsis when it fails.
A
Esophageal wall will expand upon lodging of food in esophagus. Baroceptors are activated. Another contractile wave RIGHT ABOVE the lodged bolus is initiated, generating a secondary esophageal peristalsis to push bolus into stomach
15
Q
Why does the lower esophageal sphincter relax first and then contract?
A
It relaxes to let food enter fundus of stomach. It contracts soon after to prevent reflux of food back into esophagus.
16
Q
What are the 4 anti-reflux mechs
A
- High tone of lower esophageal sphincter (note that MOST of the time, LES is closed. Only opens for swallowing)
- Secondary esophageal peristalsis. Baroceptors may/may not be activated. BUT, CHEMOCEPTORS WILL FOR SURE ALWAYS BE ACTIVATED because esophagus is sensitive to acid. This will then trigger the secondary esophageal peristalsis.
- Pinching of lower esophageal sphincter by diaphragm. Anatomical adaptation. Diaphragm sits at level of LES. It consequently pinches it.
- Reflexes (lower esophageal sphincter contracts in response to gastric and abdominal pressure increases…hugging will do this)
17
Q
What anti reflexes do infants have/not have?
A
Infants: take time to develop LES high tone, lack secondary esophageal peristalsis, lacks LES closing reflex induced by pressure buildup in gastric and abdominal areas. INFANT STILL HAS PINCHING EFFECT BY DIAPHRAGM.
18
Q
What anti reflexes do pregnant women have/not have?
A
Hormonal changes in body screw up their high tone of LES (consider it gone). However, they still have secondary esophageal peristalsis. They do NOT have pinching of LES by diaphragm (it is weakened), especially during the 3rd trimester because of uterus elevation, subsequently raising level of diaphragm. Reflex induced by increased gastric and abdominal pressure is also weakened. All of these contribute to higher instances of heartburn in pregnant women.
19
Q
Gastroesophageal reflux disease.
A
Problem of improper LES contraction. There is overall insufficient contraction and the presence of heartburn due the failure of our esophageal wall to handle the gastric acid.
20
Q
Esophageal achalasia
A
Presence of excessive contraction due to overactive excitatory neuron or abnormal muscle overgrowth (solution = surgery). Patient may also have difficulties in swallowing
21
Q
Describe storage function of gastric motility. What are the 2 mechs?
A
This occurs in digestive period. Storage occurs in proximal (upper) stomach due to relaxation of stomach muscle.
- Receptive relaxation (during swallowing…stomach relaxes in anticipation for the arrival of the bolus.)
- Accommodation (relaxation in response to distension by food (already in the stomach).) Remember that there may be significant volume expansion but expect little wall tension increase because of high elasticity of smooth muscle.
22
Q
What the function of gastric motility, besides storage?
A
- Mixing (lower stomach): Contraction. Note: Bolus + gastric secretion = chyme
- Size reduction (lower stomach): contraction (break food small enough for emptying)
- Emptying: contraction
- Housekeeping: interdigestive period
23
Q
Explain gastric contractions during digestive peri
A
- After we eat, food is stored in proximal stomach. Stored food triggers vago-vagal reflex…Corpus Pacemaker (3.7 ECAs/min). Ach and Gastrin is also produced and delivered to the muscle cells.
- Contraction wave starts, going across fundus wall and down towards thy pyloris.
- Anything small enough will pass through the pylorus. Propulsion (consisting of mixing, size reduction, and emptying) occurs here. Freq of emptying is 0-3.7 times/min
- Both pyloris and antrum close off, trapping the content and grinding it….size reduction.
- Retropropulsion occurs, consisting of mixing and size reduction. It’s very effective.
24
Q
Which occurs first? Emptying or antral systole (grinding + retropulsion)
A
Emptying! Note that ECA occurs 3.7 (so, 4) times a min. We can empty up to 4 times a minute, but never more than that. Can be 0, 1, 2, etc.
25
Explain the kinetics of gastric emptying.
1. Meal water empties really quickly since fluids follow gravity
2. The extra fluids present in gastric emptying comes from extra stomach secretions. His stomach actually brings in much for gastric fluids than water into the lumen.
3. Solids take longer to empty (2-3 hours) since food has to be broken down into pieces small enough to pass into small intestine. Also, there are additional emptying mechs that control this.
26
Describe the forces that control gastric emptying
1. Emptying rate deals with the pushing force and anti-pushing force.
2. Emptying force: Major contributor = LOWER STOMACH PERISTALSIS. Side contributor = Upper stomach tone.
3. ANti-pushing force = PYLORIC SPHINCTER TONE + Duodenal contraction (even in terms of contribution)
27
Describe process of INCREASED gastric emptying.
1. Food enters stomach (fundus first)
2. Stretch receptors are activated, triggering vagal afferents to contact CNS
3. Vagal efferents generate Ach, stimulating stomach smooth muscle.
4. Pepsidase in the stomach (pepsinogen was inactive form) starts eating up proteins in chyme. The degraded proteins and AA's along with the vagal afferents, trigger Gastrin release
5. Gastrin (excitatory enzyme) increases turning of stomach muscles.
6. The increased pushing force moves chyme into duodenum
28
Describe process of DECREASED gastric emptying
1. In duodenum, H+ ions activate chemoceptors and stimulate S cells to release secretin.
2. Peptides from stomach + AA generated by proteases from pancreases stimulate the production of CCK. Note that lipids can also cause CCK secretion. Lipids (FFA) have stronger effect of causing CCK release.
3. Glucose from the food/digestive enzymes, that is now in the duodenum, resulting in GIP production. SO Secreitin, GIP, and CCK all help make dueodeum area contract, reating resistanc and inhibiting gastrin, and tcus reducing the pushing force
4. Content inside duodenum trigger stretch receptors, strengthening pyloric sphincter contraction and relaxing stomach muscles.
29
What is special about contents within the duodenum?
As long as contents are in the duodeunum, the Secretin, GIP, and CCK will keep being secreted, and emptying of the gastric contents from the stomach WILL be slowed. When food is not in the duodenum, you get faster emptying.
30
Describe interdigestive period of digestion. Compare MMC waves during digestion vs interdigestion
Deals with STRONG peristaltic waves (MMC) to take care of hosuekeekking. Essentially, you get stronger contractions when the stomach is empty.
Digestion: low, constant MMC waves
Interdigestion: Thicc, spiked pulsating waves.
31
Desvirbe pyloris during digestive period and MMC (interdigestion) period
Digestive: Sphincter is closed during digestive motility period. Narrow opening (0.2 mm). Slows down digestion and optimizes absorption. Motilin is gone. All that is present is Gastrin, among other endocrines and paracrines.
Interdigestive: Pyloris has zero constriction. It's busted wide open. Motilin hormone is present. Also, contractive waves + pyloric sphincter work together to allow emptying of large pieces into intestine.
32
What is purpose of having a small pyloris during digestive period?
Makes sure that the gastric contents go into intestine in a orderly fashion at a reasonable slow speed. Allows for optimum digestion and absorption.
33
Dumping syndrome
There is no controled gastric emptying...everything is dumped into the intestine at once.
34
Describe muscularis externa in small intestine
1. Controls intraluminal MIXING and PROPULSION by SEGMENTATION, and optimizes digestion and absorption.
2. It deals with housekeeping (through MMC
35
Describe muscularis mucosa and villus muscle in small intestine.
Facilitates absorption and lympth flow. Their contractions are NOT sufficient to move the luminal contents.
36
Another name for segmentation
Slow movement
37
Describe what segmentation is.
It's the separation and recombining of chyme boluses.
1. When you mix the chyme with secretions (enzymes, alkaline fluids, bile), this is called luminal digestion.
2. When you engage the chyme wit cell membrane with digestive enzymes, you get membrane enzymes. If you engage it with transporters and carriers, you a get absorption. All of this stuff in total happens as a result of segmentation. You need to know this entire card.
38
What are ECAs?
Electric Control Activities. They facilitate smooth muscle contractions in the gut. AKA slow waves aka electric rhythms. They are generated by pacemaker cells. Pacemaker cells have different frequencies, depending on region. ECAs are generated spontaneously and constantly. Whether or not you have a contraction, you will always have an ECA. They are conducted to smooth muscles and through gap junctions between the muscle. Motor neurons in the smooth muscle modulates, but DO NOT INITIATE ECAs.
39
Describe pacemaker rhythm for:
1. Stomach:
2. Duodenum:
3. Ileum:
4. Colon:
1. Stomach: 3 ECAs per minute
2. Duodenum: 12 ECA per minute
3. Ileum: 10 ECA per minute
4. Colon: 3 ECA per minute
40
How do you initaite an ECA?
1. Depol a Ca and an Na channel. you need both!
2. Expect plateau phase as rate of Ca and Na influx decreases and K efflux starts to increase
3. Repol phase, which is entirely K efflux.
This whole process is voltage dependent.
41
What affects ECA aestetic?
Size of ECA varies according to neuroendocrines present in muscle. You need MORE stimulatory neuroendocrine and less inhibitory ones. If you have inhibitory and not stimulatory, expect it to be small. If you have stimulatory and no inhibitory, it will be large (since more Na and Ca channels would be activated), but you won't see spikes (last requirement). You need a crap ton of stimulatory neuroendocrines to get the spikes present.
42
Which ECA's cause muscle contractions?
LARGE ECA's with SPIKE POTENTIALS cause motor contractions. Small ECAs do not.
43
What is the name of an ECA with spikes?
ERA (electrical response activity), because it can actually make the muscle contract. NOTE: ERA frequency determines the frequency of contraction!!!
44
What excitatory neuroendocrine is used to stimulate an ERA? Inhibit it?
1. Ach
| 2. Norepi, NO
45
When superimposing an ERE to an esophagus, where would they fit, and how would it look with and without a stimualtory or inhibitory neuroendocrine?
Esophagus is straight. ANy time there is a narrowing of the esophagus, it means that the CIRCULAR muscle contracted due to the presence of an ERA. It also means that the longitudinal muscles relaxed in that same corresponding area. In widened portion of esophagus, longitudinal muscle are contracting, circular muscles are relaxing, and ERA is not present (norepi instead of the stimulatory agent Ach is). Note: there will always be MORE INHIBITORY neuroendocrines IN FRONT of the bolus. More excitatory neuroendocrines in the back of it in order to create propulsion.
46
What is the goal of creating electrical response activities?
Generates pressure through esophagus, which follows path of least resistance (towards stomach).
47
What coordinates pressure gradient formed in esophagus?
INTERNEURONS.
1. Bolus delivers mechanical stretch signals. The can be mechanical (due to stretching, calls in baroceptors), osmotic (due to salty foods, calls in osmoceptors), or can be chemical (due to spicy food. Calls in chemoceptors.)
2. All the signals are sent to interneuron, which determines if excitatory neuroendocrine is released to proximal end (contraction) or inhibitory neuroendocrine should be sent to distal esophagus (relaxation).
3. Bolus follows pressure gradient.
48
Describe Segmentation contractile behavior.
Short distance propulsion. Net movement is still forward, but a significant amount is still propelled backwards. Occurs in digestion period.
49
Describe migrating myoelectric complexes (MMC) contractile behavior.
Intermediate distance propulsion. Better coordination of contractions and relaxations than segmentation.
50
Describe diarrhea/vomiting contractile behavior.
GI wall over-secretes luminal fluids, stretches the well. You have VERY WELL coordinated neuroendocrine activities in that nearly everything moves downwards in diarrhea or upwards in vomiting. Both are long distance propulsion, although vomiting is technically reverse propulsion mechs. Exotoxins causes diarrhea.
51
What is the ileo-cecal sphincter?
Separates the large intestine from the small intestine. Takes care of reflexive relaxation and contraction strictly in response to gestation at either end (ceal or ileum).
52
What is the job of the large intestine?
Takes care of haustral shuttling and mass movements.
53
Job of rectum?
Defacation
54
What is the job of the phasic and tonic contraction of the ileo-cecal sphincter?
Tonic contraction: removes chyme from ileum into the cecum.
| Phasic contraction: makes sure no mass returns back into the ileum.
55
What happens if you distend the distal ileum with pressure (chyme, for instance)?
1. Ileo-cecal sphincter relaxes
| 2. Chyme enters into cecum.
56
What happens if you distend the proximal cecum with pressure (or fecal matter)?
1. Ileo-cecal sphincter closes
| 2. Reflux of fecal matter back into the ileum is prevented
57
What kind of motility is demonstrated in the large intestine? Describe it.
Haustral shuttling: segmenting nonperistaltic contraction to slow fecal stream. Essentially, relatively weak contractions designed for storage of fecal material. Note that there are occasional peristaltic activities to push stool through colon.
58
What happens to the 700 ml of water that makes its way to the cecum?
Water and electrolytes are reabsorbed into the interstitium.
59
What is retrograde (oral propulsion)?
Fecal matter moving in opposite direction in colon. Used to store stool longer.
60
Mass movement
Sustained peristaltic wave used to push stool to rectum and initiate defecation.
61
What is the resting position of inner and outer rectal sphincters?
```
Inner sphincter (involuntary): contracted
Outer sphincter (voluntary): relaxed.
```
62
Describe reflex that occurs once fecal matter reaches the inner sphincter.
1. Pressure builds
2. Inner sphincter opens.
3. Outer sphincter closes.
4. Signal sent to brain to make decision to withhold or release fecal matter.
63
What causes in increase in the urge for defecation?
Enteric NS and CNS shuttle more and more fecal matter to the rectum, building up more and more pressure onto the inner sphincter, increasing more and more awareness to the brain of the need to defecate. Note that voluntary control to withhold fecal matter can still be applied.
64
True or false: The urge for defecation will last until you actually release the fecal matter.
False. The urge to defecate is only temporary. After a given period of time, retro (oral) propulsion pushes the fecal matter back into area of transverse colon and further back.
65
Describe general defecation habits.
Generally dietary and culturally defined. Some eat less, some eat more. Those who eat less, defecate less. Diets high in fiber lead to more frequent defecation. Citizens in cultures more accepting of defecation will also defecate more.
66
Consequences of increased defecation:
Diarrhea = increased defecation. life threatening since it leads to dehydration.
67
Consequences of decreased defecation:
Only leads to displeasure. Longest known length during which one went without defecation was 3 months...needed to be surgically removed. Infrequent defecation may or may not be linked to colon cancer. Note that constipation is common in this society
68
List the factors that lead to constipation. There are 6 of them.
1. Diets low in soluble fiber, leading to insufficient stimulation of baroceptors. There also be a loss of microbes associated with diets high in fiber.
2. Waiting too long to defecate. This increases time spent for water reabsorption and increased haustral shuttling, resulting in dryer feces...higher resistance. This also decrease baroceptor activity due to reduced fecal volume.
3, Overuse of narcotics: These drugs inhibit GI fluid secretion, which decreases baroceptor activity...less volume = less pressure. Narcotics also increase sphincter tones, which increases resistance in the colon.
4. Physical inactivity: They tend to eat less, which decreases fecal mass, and thus decreases baroceptor activity. The patients also have decreased GI neuroendocrine activity associated with exercise (exercise more = increased neuroendocrine activity)
5. Antibiotic use: leads to loss of gut microbiome-initiated enteric nervous system activities. But note that this can also cause diarrhea. Depends on antibodies and bacteria you have.
6. Old age: elderly eat less and have reduced neuroendocrine and physical activities. This is the one factor that is hard to reverse.
69
Describe gastroileal reflex
Long distance, stimulatory reflex. Entry of food into the EMPTY stomach results in relaxation of ileo-cecal sphincter, leading to the emptying of the ileum.
70
Describe gastrocolic reflex/ duodenocolic reflex
Long distance, stimulatory reflex. Entry of food into the EMPTY stomach OR chyme into the duodenum results in increases of aboral propulsive movement (as in, movement further away from the mouth) in the colon.
71
Colonocolonic reflex
Long distance, stimulatory reflex. Distension of one part of the colon leading to relaxation of other parts ( final result is decreased resistance and increased aboral movement)
72
When are colonic reflex muscles strongest? Before or after feeding?
After feeding.
73
Duodenogastric reflex
Long distance, Inhibitory reflex. Duodenal distension causes decreased gastric emptying.
74
Ileogastric reflex
Long distance, Inhibitory reflex. Ileal distension leads to decreased gastric emptying. Note that if you have an ileum resection, you lose this reflex, and thus increase gastric emptying, shortening gastric storage time.
75
Intestino-intestinal reflex. Pathophysiological
Long distance, Inhibitory reflex. Over-distension of a segment of intestine caused by intestinal obstruction (due to strictures, adhesions, cancer, irritable bowel syndrome, etc) results in a generalized inhibition of intestinal muscle activity.)
76
Colonic-intestinal reflex. Pathophysiological
Long distance, Inhibitory reflex. Over-distension in the colon caused by obstruction (due to strictures, adhesions, cancer, irritable bowel syndrome, etc) results in a generalized inhibition of intestinal muscle activity.)
77
Peritoneo-intestinal reflex (adynamic ileus). Pathophysiological
Long distance, Inhibitory reflex. Handling of the intestine during abdominal surgery or peritoneal irrigation results in a generalized inhibition of intestinal muscle activity. This is why you are asked not to eat or drink after a major surgery or irrigation. If they do eat, food will sit there in body, bacteria will germinate, and patient will get really gassy.
78
How do you know a patient has regained GI motility after a surgery?
Ask them if they farted. Note that the gas comes from blood gases and bacteria. You wouldn't ask them i they defecated because that is usually cleaned out in gi surgery. You wouldn't listen for borborigmi sounds because patient would not know. You would not use barium x-ray because you don't want to use barium on a patient who just had surgery. You would not use GI endoscopy either because endoscopy can't check for GI motility.
